Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Abstract

Olfactory bulb glomeruli are formed by a network of three major types of neurons collectively called juxtaglomerular (JG) cells, which include external tufted (ET), periglomerular (PG), and short axon (SA) cells. There is solid evidence that γ-aminobutyric acid (GABA) released from PG neurons presynaptically inhibits glutamate release from olfactory nerve terminals via activation of GABA B receptors (GABA B -Rs). However, it is still unclear whether ET cells have GABA B -Rs. We have investigated whether ET cells have functional postsynaptic GABA B -Rs using extracellular and whole cell recordings in olfactory bulb slices. In the presence of fast synaptic blockers (CNQX, APV, and gabazine), the GABA B -R agonist baclofen either completely inhibited the bursting or reduced the bursting frequency and increased the burst duration and the number of spikes/burst in ET cells. In the presence of fast synaptic blockers and tetrodotoxin, baclofen induced an outward current in ET cells, suggesting a direct postsynaptic effect. Baclofen reduced the frequency and amplitude of spontaneous EPSCs in PG and SA cells. In the presence of sodium and potassium channel blockers, baclofen reduced the frequency of miniature EPSCs, which were inhibited by the calcium channel blocker cadmium. All baclofen effects were reversed by application of the GABA B -R antagonist CGP55845. We suggest that activation of GABA B -Rs directly inhibits ET cell bursting and decreases excitatory dendrodendritic transmission from ET to PG and SA cells. Thus the postsynaptic GABA B -Rs on ET cells may play an important role in shaping the activation pattern of the glomeruli during olfactory coding.

Lack of functional GABAB receptors alters GnRH physiology and sexual dimorphic expression of GnRH and GAD-67 in the brain

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Two GABAergic Intraglomerular Circuits Differentially Regulate Tonic and Phasic Presynaptic Inhibition of Olfactory Nerve Terminals

“…These results do not exclude the possibility of additional tonic GABA B R inhibition at the ET3 PG synapse. However, while a recent study showed that ET cells have GABA B Rs that can be activated by exogenous baclofen, ET cells showed no evidence of tonic inhibition by endogenous GABA (Karpuk and Hayar 2008). This suggests that the tonic inhibition across the ON3 ET3 PG circuit is primarily due to tonic GABA B R inhibition at the ON3 ET synapse.…”

Neuroinflammation Leads to Region-Dependent Alterations in Astrocyte Gap Junction Communication and Hemichannel Activity

“…The use of I–V slopes represents the most precise method to calculate input conductance or resistance, since several recordings with different voltages and currents are included into the linear regression algorithm, which minimizes calculation errors (Karpuk and Vorobyov, 2003; Mishima et al, 2007; Karpuk and Hayar, 2008). Cell membrane capacitance (Cm) was calculated using the definition of time constant, t=RC, where t was the time constant calculated by the declining membrane potential at 5–20 mV from resting membrane potential (RMP) (i.e.…”